The main objective of the present experiment was to investigate whether progesterone priming eliminates defective luteal function in seasonally anoestrous ewes induced to ovulate with pulsatile GnRH treatment by synchronizing the early stages of follicle development. This was achieved by suppressing and synchronizing the early stages of follicle development with bovine follicular fluid (bFF) and then investigating whether this was sufficient to eliminate defective luteal function following the induction of ovulation with GnRH. Ewes in group 1 (no. = 10) were injected s.c. with 2 ml bFF at 8-h intervals for a period of 3 days before the start of GnRH treatment. Animals in group 2 (no. = 10), ivhich served as positive controls, were given a single i.m. injection of 20 mg progesterone 3 days before the start of GnRH treatment, while those in group 3 (no. = 10), which served as negative controls, were injected with corn oil alone at this time. Ewes in all the three groups were induced to ovulate by administration of 2-hourly injections of GnRH (250 ng per injection) for 54 h. Frequent blood samples for LH, FSH, and oestradiol were collected around the time of both progesterone/bFF injections and GnRH treatment, as well as daily thereafter to monitor luteal function.

The bFF injections given to animals in group 1 resulted in a significant (P<0·001) suppression of FSH concentrations, followed by a rebound rise in concentrations after the cessation of treatment. GnRH treatment significantly (P < 0·05) increased both mean LH pulse amplitude and overall mean LH concentrations in all the three groups, while LH pulse frequency was increased only in non-bFF-treated ewes. Plasma oestradiol concentrations 24 h after the start of GnRH treatment were significantly (P < 0·05) higher in groups 2 and 3 compared with group 1. These differences in the patterns of oestradiol concentrations over time were associated with a significant (P <0·05) delay in the onset of the pre-ovulatory LH surge in ewes treated witli bFF (group 1). However, there was no difference in either the duration or the height of pre-ovulatory LH surge between the three treatment groups. Ewes in all three treatment groups ovulated in response to GnRH treatment. However, both laparoscopic examination and plasma progesterone concentrations revealed that the incidence of normal luteal function was significantly (P < 0·05) higher in group 2 (10/10) compared with groups 1 (2/10) and 3 (4/10), with no difference between groups 1 and 3. Overall, these results suggest that progesterone priming does not eliminate defective luteal function through synchronizing early stages offollicle development.

The main objective of the experiment was to investigate the mechanism by which progesterone priming eliminates defective luteal function in anoestrous ewes induced to ovulate with GnRH. Animals in group 1 (no. = 10) were primed with a single i.m. injection of progesterone in corn oil 3 days before the start of GnRH treatment, while ewes in group 2 (no. = 10) received corn oil alone and served as untreated controls. Ewes in group 3 (no. = 10), which served as positive controls, were treated with an intra-vaginal progestagen sponge for 7 days, and this was removed just before the start of GnRH treatment. Ewes in all three groups were induced to ovulate by administration of 2-h injections of GnRH (250 ng per injection) for 54 h. Frequent blood samples for LH, FSH and progesterone analysis were taken around the time of both progesterone injection and GnRH treatment, as well as daily thereafter to monitor luteal function, and laparoscopy was performed 3 and 7 days after GnRH treatment.

The incidence of ovulation was similar for all the three groups (8/10, 7/10 and 9/10 for groups 1, 2 and 3 respectively). Hoioever, both laparoscopic examination and plasma progesterone concentrations revealed that the incidence of normal luteal function was significantly higher in progesterone-primed animals group 1:7/8; group 3:9/9) compared ivith controls (group 2:0/7), P < 0-05) with no difference between groups 1 and 3. Injection of progesterone on day −3 significantly suppressed mean LH concentrations (P < 0·05), but mean FSH concentrations were not altered. However, there were no significant differences between groups in LH and FSH concentrations over the period of GnRH treatment, nor in the timing, duration and height of pre-ovulatory LH and FSH surges. These results suggest that progesterone priming may eliminate defective luteal function either by changing LH concentrations at the time of progesterone administration or through mechanisms not involving gonadotropin secretion.